European journal of gynaecological oncology最新文献

{"title":"CELSR1 enhances doxorubicin resistance by activating the WNT/PCP signaling pathway in breast cancer cells","authors":"","doi":"10.22514/ejgo.2024.096","DOIUrl":"https://doi.org/10.22514/ejgo.2024.096","url":null,"abstract":"Doxorubicin (Dox) is a widely used chemotherapy drug to inhibit the growth and survival of human breast cancer (BC) cells. Presently, there is a pressing need for the development of new therapeutic strategies to enhance Dox efficacy by overcoming the resistance exhibited by breast cancer cells. Cadherin EGF LAG seven-pass G-type receptor 1 (CELSR1), belonging to the Flamingo subfamily, has been implicated in the progression of various tumors. However, the specific role and mechanisms of CELSR1 in the resistance of breast cancer to drug treatments have yet to be fully understood. This study aims to clarify the role of CELSR1 in conferring resistance to doxorubicin in breast cancer. Our findings demonstrate that CELSR1 expression is elevated in breast cancer tissues. Silencing of CELSR1 significantly reduced the proliferation and motility of breast cancer cells. Moreover, the ablation of CELSR1 decreased the resistance of breast cancer cells to doxorubicin treatment. At the molecular level, CELSR1 was found to activate the Wnt/Planar Cell Polarity (WNT/PCP) signaling pathway in breast cancer cells. In conclusion, CELSR1 plays a crucial role in promoting the migration of breast cancer cells and in enhancing their resistance to doxorubicin through the activation of the WNT/PCP pathway.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 5","pages":"91-91"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147889895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CRMP4 suppresses cervical cancer cell proliferation and EMT through the Wnt/β-catenin pathway","authors":"","doi":"10.22514/ejgo.2024.102","DOIUrl":"https://doi.org/10.22514/ejgo.2024.102","url":null,"abstract":"Cervical cancer is the 4th leading cause of tumor-related deaths among women, primarily due to high-risk Human Papillomavirus (HPV). The role of Collapsin Response Mediator Protein 4 (CRMP4) in cervical cancer remains poorly understood, despite its variable expression across various cancers. This study aimed to investigate the mechanisms by which CRMP4 regulates cervical cancer cell growth as well as Epithelial-Mesenchymal Transition (EMT). Based on transcriptome data from The Cancer Genome Atlas (TCGA), CRMP4 is significantly downregulated in cervical cancer tissues compared to normal tissues. Immunoblot assays revealed lower CRMP4 expression in cervical cancer cell lines. Cell Counting Kit-8 (CCK-8), colony formation and flowcytometry demonstrated that CRMP4 overexpression inhibited cell growth as well as stimulated apoptosis in HeLa as well as SiHa cells. In addition, CRMP4 overexpression increased Epithelial cadherin (E-cadherin) levels and decreased Neural cadherin (N-cadherin) and alpha-Smooth Muscle Actin (α-SMA) levels, indicating EMT suppression. CRMP4 overexpression downregulated the Wnt/β-catenin axis by reducing expressions of β-catenin, Wnt family member 3A (Wnt3a), c-Myc and cyclin D1. In summary, CRMP4 inhibits cervical cancer cell proliferation as well as EMT by mediating the Wnt/β-catenin axis. CRMP4 may therefore be a potential therapeutic target of cervical cancer.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 5","pages":"146-146"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147914784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ketamine inhibits endometrial cancer cell growth and motility by inducing ferroptosis","authors":"","doi":"10.22514/ejgo.2024.075","DOIUrl":"https://doi.org/10.22514/ejgo.2024.075","url":null,"abstract":"Endometrial cancer (EC) is a prevalent gynecological malignancy with an escalating incidence and mortality rate, notably in China. Surgical options are limited, and drug resistance development poses significant challenges to EC treatment. Ketamine, a rapid-acting anesthetic, exhibits anti-inflammatory, analgesic, and antidepressant properties, yet its potential in cancer therapy remains largely unexplored. Here, we investigate ketamine’s effects on EC cell growth, motility and ferroptosis, alongside its impact on the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/the mammalian target of rapamycin (mTOR) axis. Ketamine significantly inhibits EC cell growth and motility while promoting ferroptosis. Mechanistically, ketamine’s anti-tumor effects correlate with suppression of the PI3K/Akt/mTOR axis crucial for cell survival and growth. In summary, our findings highlight ketamine’s potential therapeutic application in EC treatment by impeding cell growth and motility, fostering ferroptosis, and suppressing the PI3K/Akt/mTOR axis. These insights offer novel avenues for EC therapy.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 4","pages":"110-110"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147898143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sauchinone inhibits the growth and epithelial-mesenchymal transition of ovarian cancer cells","authors":"","doi":"10.22514/ejgo.2024.133","DOIUrl":"https://doi.org/10.22514/ejgo.2024.133","url":null,"abstract":"Ovarian cancer (OC) is a common malignant reproductive tumor among women that adversely affects their health. It has been proven that Sauchinone (Sau) derived from Saururus chinensis (Lour.) Baill may aid tumorigenesis in diversiform cancers. Despite this, the regulatory impact of Sau on OC progression remains unclear. In this study, firstly, Sau (10 or 20 µM) had been confirmed to possess no cytotoxicity, so Sau (10 or 20 µM) was utilized for the next experiments. Sau was shown to prevent cell growth in OC. Furthermore, Sau inhibited cell migration and invasion in OC. Our findings demonstrated that Sau attenuated the epithelial-mesenchymal transition (EMT) process by elevating E-cadherin and declining N-cadherin and alpha-smooth muscle actin (α-SMA) expressions. Lastly, Sau blocked the wingless/integrated (Wnt)/β-catenin pathway. In summary, Sau inhibited cell growth, EMT, and blocked the Wnt/β-catenin pathway in OC progression. Sau may offer novel perspectives on OC treatment in this study.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 6","pages":"190-190"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147907212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"APOBEC3G inhibits apoptosis and autophagy in cervical intraepithelial neoplasia W12 cells","authors":"","doi":"10.22514/ejgo.2024.101","DOIUrl":"https://doi.org/10.22514/ejgo.2024.101","url":null,"abstract":"Cervical intraepithelial neoplasia (CIN) is a collective term for specific precancerous lesions associated with cervical cancer (CC). Given the current poor prognosis, it is imperative to diagnose CIN at an early stage and identify the markers linked to its pathogenesis and prognosis, despite the disease’s documented slow course and numerous levels of cellular alterations. We explored the expression level of the new marker apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G, A3G) and its regulatory effect on CIN. Cell proliferation were assessed using Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2′-deoxyuridine (EdU) staining. Apoptosis rate was detected by flow cytometry. We used immunofluorescence to determine light chain 3B (LC3B) expression. Western blotting was used to detect Bcl2-Associated X (Bax), B-cell lymphoma 2 (Bcl-2), Cleaved caspase-3, p62, LC3-II/LC3-I, transforming growth factor-beta (TGF-β) and decapentaplegic homolog 2 (Smad2) expressions. A3G knockdown significantly inhibited cervical intraepithelial neoplasia cell proliferation, significantly increasing the apoptosis rate and the Bax/Bcl-2 ratio. Also, Cleaved-caspase-3 and LC-II expressions were significantly increased, and p62 expression was decreased. The TGF-β/Smad2 signaling pathway was significantly inhibited. In cervical intraepithelial neoplasia, APOBEC3G inhibits apoptosis and autophagy of W12 cells through TGFβ/Smad2 signaling pathway. In conclusion, we determined that APOBEC3G has a regulatory effect on CIN, which opens a new way to explore its pathogenesis and improve the accuracy of prognosis.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 5","pages":"140-140"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147917001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Taraxasterol inhibits cell proliferation and angiogenesis in ovarian cancer by targeting EphA2","authors":"","doi":"10.22514/ejgo.2024.049","DOIUrl":"https://doi.org/10.22514/ejgo.2024.049","url":null,"abstract":"Ovarian Cancer (OC) is a prevalent gynecological malignancy, underscoring the urgency to discover novel therapeutic approaches that enhance both clinical efficacy and safety. Taraxasterol (TA), an important component of dandelion, has been reported to exhibit inhibitory effects on the progression of various tumors. However, its specific role in OC is yet to be reported. In this present study, we observed that TA significantly inhibits the proliferation of OC cells, promotes apoptosis and reduces OC cell migration and angiogenesis. Mechanistically, TA targets the EPH receptor A2 (EphA2) receptor, thereby inhibiting OC progression. In conclusion, the ability of TA to suppress both cell proliferation and angiogenesis in OC through EphA2 targeting suggests its potential utility as a therapeutic agent for OC.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 3","pages":"62-62"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147882627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpression of URG11 can inhibit the proliferation and motility of breast cancer cells","authors":"","doi":"10.22514/ejgo.2024.052","DOIUrl":"https://doi.org/10.22514/ejgo.2024.052","url":null,"abstract":"Breast cancer (BC) is the most common type of cancer among women worldwide, and identifying the key molecules that regulate cell metastasis is essential to improve the patients’ prognosis and developing potential therapeutic strategies. Upregulator gene 11 (URG11) plays a significant role in cancer cell motility. Despite its relevance, its role and underlying mechanism in BC remains underexplored. This study aimed to investigate the significance and mechanism of action of URG11 in BC. The results indicated a low expression of URG11 in BC and revealed that its overexpression could suppress BC cell growth and motility. Through mechanistic studies, we discovered that URG11 overexpression inhibited the Wnt/β-Catenin pathway in BC cells. In summary, URG11 overexpression could inhibit the growth and motility of BC cells by suppressing the Wnt/β-Catenin pathway, suggesting URG11 as a potential target for BC management.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 3","pages":"88-88"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147881104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting CENPN to inhibit breast cancer progression: insights into cell growth and aerobic glycolysis modulation","authors":"Zhe Ye, Qiuyan Lin, Hualong Lin, Yiwei Huang, S Winters, C Martin, D Murphy, N Shokar, K Miller, L Nogueira, T Devasia, A Mariotto, K Yabroff, A Jemal, S Krmer, C Rogmans, D Saylan, D Friedrich, C Kraft, G Rogmans, D Crosby, S Bhatia, K Brindle, L Coussens, C Dive, M Emberton, R Cairns, I Harris, T Mak, A Orang, J Petersen, R Mckinnon, M Michael, M Vander Heiden, L Cantley, C Thompson, J Cantor, D Sabatini, Y Feng, Y Xiong, T Qiao, X Li, L Jia, Y Han, Z Schug, Vande Voorde, J Gottlieb, E, S Lunt, Vander Heiden, M, J Park, W Pyun, H Park, Z Wu, J Wu, Q Zhao, S Fu, Jin, K Su, M Tsang, N Emans, I Cheeseman, S Chittori, J Hong, H Saunders, H Feng, R Ghirlando, A Kelly, Y Zheng, H You, J Duan, B Chen, C Wu, P Chen, S Xu, X Wei, C Qi, M Huang, Y Zou, R Yang, Y Jiang, J Sheng, S Andres, K Bickett, M Alatoum, T Kalbfleisch, G Brock, J Wittliff, Y Wang, Y Li, B Liu, A Song, X Yang, J Gong, X Cai, Y Yuan, Y He, Q Li, W Zhou, Y Gu, Y Jiang, Y Zhang, T Wu, B Zhao, Z Liu, R Qian, J Zhang, R Chhabra, S Rao, B Kumar, A Shetty, A Hegde, M Bhandary, E Lee, J Lee, S Park, S Chun, B Yoon, J-W Chung, J Xie, Y Zhou, Y Ge, Y Huang, Y Liu, S Lian, Z Cai, Y Tang, C Wei, T An, L Guo, X Li, Y Li, X Du, X Wang, S Guan, Y Cao, L Zhang, L Wang, H Yang, C Li, C Fang, X Wang, M Lai, Y Wang, R Chai, N Li, L Ou, X Wang, K Zhang, C Fu, F Wu, J Zhang, B Han, J Han, Y Wang, R Yang, Y Xu, F Li, Y Jia, H Wu, Y Zhou, H Wu, L Xu, Y Yan, X Tong, Q Wang, X Yu, Z Zheng, F Chen, N Yang, Y Zhou, N Oka, A Kasamatsu, Y Endo-Sakamoto, K Eizuka, S Wagai, N Koide-Ishida, J Kim, Z Zhang, Z Zou, H Dai, R Ye, X Di, R Li, M Rahman, T Islam, E Gov, B Turanli, G Gulfidan, M Shahjaman, Q Yang, W Jiang, P Hou, J Li, Elk Goh, J He, Y Li, Fan Yu, Z, S Pandey, S Mondal, K Kajal, B Kurmi, S Verma, P Patel, R Malayil, Y Chhichholiya, K Vasudeva, H Singh, T Singh, S Singh, P Zhou, Z Zheng, T Wan, J Wu, C Liao, X Sun, I Robey, A Lien, S Welsh, B Baggett, R Gillies, H Yang, P Lin, C Vadivalagan, Y Lin, K Lin, Y Hseu, B Liu, X Qu, J Wang, L Xu, L Zhang, B Xu","doi":"10.22514/ejgo.2024.037","DOIUrl":"https://doi.org/10.22514/ejgo.2024.037","url":null,"abstract":"Breast cancer represents a significant health challenge for women globally. Although centromere protein N (CENPN) is reported to be upregulated in breast cancer, its detailed role remains unclear. This study used in silico analysis to investigate the expression profile and survival impact of CENPN in breast cancer. The CENPN level was evaluated using real-time quantitative polymerase chain reaction and western blot assays. The influence of CENPN on cell proliferation and aerobic glycolysis was investigated through cell counting kit-8, 5-ethynyl-2′-deoxyuridine incorporation assays, measurements of the extracellular acidification rate (ECAR), glucose uptake, lactate production, and additional western blot analyses. Moreover, in vivo studies on xenografted mice were conducted, utilizing immunohistochemistry and western blot techniques to evaluate the functions of CENPN. These findings revealed an upregulation of CENPN, correlating with decreased survival rates in breast cancer patients. Functionally, CENPN was shown to stimulate cell growth in both cell culture and animal models. Through gain- and loss-of-function experiments, CENPN was found to increase the ECAR, glucose uptake, lactate production, and the protein levels of glucose transporter 1 (GLUT1) and hexokinase 2 (HK2). Furthermore, CENPN was observed to increase the levels of phosphorylated protein kinase B (AKT) (p-AKT) relative to total AKT and hypoxia-inducible factor 1α (HIF-1α) in both cellular and animal models. The HIF-1α overexpression mitigated the suppressive effects of sh-CENPN on cell proliferation and aerobic glycolysis in breast cells. In conclusion, CENPN is upregulated and is related to a lower survival probability in breast cancer. It facilitates cell growth and aerobic glycolysis by upregulating AKT/HIF-1α signaling pathways. These insights provide novel perspectives for the diagnosis and treatment of breast cancer.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 2","pages":"147-147"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://oss.ejgo.net/files/article/20240415-837/pdf/EJGO2024022201.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147893091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polygonatum sibiricum polysaccharide inhibits the proliferation of endometrial cancer cells by promoting cell death","authors":"","doi":"10.22514/ejgo.2024.054","DOIUrl":"https://doi.org/10.22514/ejgo.2024.054","url":null,"abstract":"Endometrial cancer (EC) is a type of malignant tumor with increasing global incidence and mortality rates, especially in regions with high rates of obesity. Polygonatum sibiricum polysaccharide (PSP) has shown promise in addressing deficiencies associated with EC. While PSP has demonstrated anti-cancer properties across various cancer types, its efficacy in EC remains underexplored. This study investigates the inhibitory effects of PSP on EC cell proliferation and autophagy. Our data demonstrate that PSP effectively inhibits the growth of EC cells and induces apoptosis. Furthermore, PSP triggers autophagy in EC cells. Mechanistically, PSP suppresses the Toll-like receptors (TLR4)/Signal Transducer and Activator of Transcription 3 (STAT3) pathway, thereby inhibiting EC progression. In conclusion, our findings highlight the significant therapeutic potential of PSP in EC treatment by inhibiting cell growth, inducing apoptosis, and triggering autophagy via the TLR4/STAT3 pathway.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 3","pages":"114-114"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147888494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KIF2C promotes doxorubicin resistance in ovarian cancer cells and increases cancer cell glycolysis by upregulating PKM2","authors":"","doi":"10.22514/ejgo.2024.129","DOIUrl":"https://doi.org/10.22514/ejgo.2024.129","url":null,"abstract":"Ovarian cancer stands as one of the most frequently diagnosed malignant tumors among women. Doxorubicin (DOX), a potent anthracycline chemotherapeutic agent, is widely used in the treatment of ovarian cancer. However, resistance to DOX remains a significant challenge. Kinesin family member 2C (KIF2C), a member of the Kinesin-13 family, has been associated with various cancers, but its specific involvement in the resistance of ovarian cancer to DOX remains to be elucidated. This study investigates the role of KIF2C in ovarian cancer DOX resistance. Through meticulous experimentation, we successfully constructed two DOX-resistant ovarian cancer cell lines and found that KIF2C was overexpressed in these cells, promoting cell growth. By silencing KIF2C, we were able to re-sensitize the DOX-resistant cells to the drug and significantly impair their migratory capabilities. Our mechanistic studies revealed that KIF2C upregulates the expression of pyruvate kinase isozyme type M2 (PKM2), thereby enhancing glycolysis—a key metabolic pathway—in DOX-resistant ovarian cancer cells. In summary, KIF2C contributes to DOX resistance and enhances glycolysis in ovarian cancer cells by upregulating PKM2, suggesting that KIF2C may serve as a promising therapeutic target for circumventing drug resistance in ovarian cancer treatments.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 6","pages":"157-157"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147905345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}